Small-conductance Ca21-dependent K1 channels activated by ATP in murine colonic smooth muscle

Koh, S. D., G. M. Dick, and K. M. Sanders. Smallconductance Ca21-dependent K1 channels activated by ATP in murine colonic smooth muscle. Am. J. Physiol. 273 (Cell Physiol. 42): C2010–C2021, 1997.—The patch-clamp technique was used to determine the ionic conductances activated by ATP in murine colonic smooth muscle cells. Extracellular ATP, UTP, and 2-methylthioadenosine 58-triphosphate (2-MeSATP) increased outward currents in cells with amphotericin B-perforated patches. ATP (0.5–1 mM) did not affect whole cell currents of cells dialyzed with solutions containing ethylene glycol-bis(b-aminoethyl ether)-N,N,N8,N8-tetraacetic acid. Apamin (3 3 1027 M) reduced the outward current activated by ATP by 32 6 5%. Single channel recordings from cellattached patches showed that ATP, UTP, and 2-MeS-ATP increased the open probability of small-conductance, Ca21dependent K1 channels with a slope conductance of 5.3 6 0.02 pS. Caffeine (500 μM) enhanced the open probability of the small-conductance K1 channels, and ATP had no effect after caffeine. Pyridoxal phosphate 6-azophenyl-28,48-disulfonic acid tetrasodium (PPADS, 1024 M), a nonselective P2 receptor antagonist, prevented the increase in open probability caused by ATP and 2-MeS-ATP. PPADS had no effect on the response to caffeine. ATP-induced hyperpolarization in the murine colon may be mediated by P2y-induced release of Ca21 from intracellular stores and activation of the 5.3-pS Ca21activated K1 channels.